The different path of T790M-positive EGFR-mutant lung cancer

Shinkyo Yoon, Chang Min Choi, Jae Cheol Lee


Approximately half of the cases of acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) are mediated by the secondary T790M mutation (1,2). Distinct clinical course of patients with T790M-positive lung cancer has been suggested, mostly in the context of more indolent progression and favorable prognosis (3,4). It is in line with the pre-clinical study showing that EGFR-mutant cell lines with acquired T790M mutation exhibit slower growth although the way how the additional T790M mutation can affect the growth rate of EGFR-mutant lung cancer cells remains unclear (5).